Bottom Line:
Here we revisit how dietary factors could affect the treatment of patients with complications of chronic kidney disease (CKD), bringing to the attention of the reader the most recent developments in the field.We will briefly discuss five CKD-induced complications that are substantially improved by dietary manipulation: 1) metabolic acidosis and the progression of CKD; 2) improving the diet to take advantage of the benefits of angiotensin converting enzyme inhibitors (ACEi) on slowing the progression of CKD; 3) the diet and mineral bone disorders in CKD; 4) the safety of nutritional methods utilizing dietary protein restriction; and 5) evidence that new strategies can treat the loss of lean body mass that is commonly present in patients with CKD.

ABSTRACTHere we revisit how dietary factors could affect the treatment of patients with complications of chronic kidney disease (CKD), bringing to the attention of the reader the most recent developments in the field. We will briefly discuss five CKD-induced complications that are substantially improved by dietary manipulation: 1) metabolic acidosis and the progression of CKD; 2) improving the diet to take advantage of the benefits of angiotensin converting enzyme inhibitors (ACEi) on slowing the progression of CKD; 3) the diet and mineral bone disorders in CKD; 4) the safety of nutritional methods utilizing dietary protein restriction; and 5) evidence that new strategies can treat the loss of lean body mass that is commonly present in patients with CKD.

Mentions:
Do publications also document that dietary factors influence the relationship between metabolic acidosis and progression of CKD? The answer is yes because it is known that the catabolism of dietary proteins, especially if the diet supplied proteins of animal origin, is the principal source of acid generation [3]. When the kidney is challenged with acid, such as by eating an animal-source protein diet, it increases levels of hormones (i.e., angiotensin II, aldosterone, endothelin) that help it excrete the acid over short-term observations [12, 13]. However, in the long-term, high levels of these hormones worsen kidney function [14, 15]. Consequently, limiting proteins in the diet will reduce the generation of acid and should aid in the correction of metabolic acidosis. Indeed, there is evidence that protein restricted diets can also suppress the progression of CKD. For example, in 2012, these relationships were tested by Goraya and colleagues [16]. They reduced the daily amount of acid generated by simply increasing fruits and vegetables in the diet. This recommendation achieved the goal of reducing acid generation by 50 % [16]. The strategy used by the investigators simply amounted to increasing fruits and vegetables in the diet. The amount of added fruit and vegetables was based on adding what would be required for a 50 % reduction in daily acid generation. For most of the patients, this amounted to adding two to four cups of fruits and vegetables to their daily diets. In the clinical trial of the influence of adding these foods, hypertensive patients with stages 1 or 2 CKD (presumably due to hypertensive nephropathy) were treated with ACEi and outcome measures were documented [16]. The measures studied included a decrease in urinary markers of kidney damage, namely N-acetyl beta-D-glucosaminidase and TGF-β1. After 30 days, stage 2 CKD patients who were treated with either sodium bicarbonate supplements or changes in the diet designed to increase the content of fruit and vegetables had comparably positive responses estimated from decreased appearance of markers of kidney damage (Fig. 1). These positive results were obtained during studies of a small number of patients with relatively mild CKD but were sufficiently intriguing that the investigators were stimulated to undertake a larger trial [17]. In this second clinical trial, hypertensive patients with stage 4 CKD (eGFR of 15–29 ml/min/1.73 m2) and metabolic acidosis (i.e., total CO2 < 22 mM) were randomly assigned to either daily sodium bicarbonate supplements (1 mEq/kg/day) or to an increase in dietary fruits and vegetables that was sufficient to reduce dietary acid by 50 %. After 1 year of treatment, the total CO2 had increased to a similar extent (compared to baseline values) in both the sodium bicarbonate and fruits plus vegetables groups. Regarding kidney functional outcomes, the eGFR calculated from plasma cystatin C levels did not differ between the groups but indices of kidney injury were lower in patients treated with diets enriched in fruits and vegetables.Fig. 1

Mentions:
Do publications also document that dietary factors influence the relationship between metabolic acidosis and progression of CKD? The answer is yes because it is known that the catabolism of dietary proteins, especially if the diet supplied proteins of animal origin, is the principal source of acid generation [3]. When the kidney is challenged with acid, such as by eating an animal-source protein diet, it increases levels of hormones (i.e., angiotensin II, aldosterone, endothelin) that help it excrete the acid over short-term observations [12, 13]. However, in the long-term, high levels of these hormones worsen kidney function [14, 15]. Consequently, limiting proteins in the diet will reduce the generation of acid and should aid in the correction of metabolic acidosis. Indeed, there is evidence that protein restricted diets can also suppress the progression of CKD. For example, in 2012, these relationships were tested by Goraya and colleagues [16]. They reduced the daily amount of acid generated by simply increasing fruits and vegetables in the diet. This recommendation achieved the goal of reducing acid generation by 50 % [16]. The strategy used by the investigators simply amounted to increasing fruits and vegetables in the diet. The amount of added fruit and vegetables was based on adding what would be required for a 50 % reduction in daily acid generation. For most of the patients, this amounted to adding two to four cups of fruits and vegetables to their daily diets. In the clinical trial of the influence of adding these foods, hypertensive patients with stages 1 or 2 CKD (presumably due to hypertensive nephropathy) were treated with ACEi and outcome measures were documented [16]. The measures studied included a decrease in urinary markers of kidney damage, namely N-acetyl beta-D-glucosaminidase and TGF-β1. After 30 days, stage 2 CKD patients who were treated with either sodium bicarbonate supplements or changes in the diet designed to increase the content of fruit and vegetables had comparably positive responses estimated from decreased appearance of markers of kidney damage (Fig. 1). These positive results were obtained during studies of a small number of patients with relatively mild CKD but were sufficiently intriguing that the investigators were stimulated to undertake a larger trial [17]. In this second clinical trial, hypertensive patients with stage 4 CKD (eGFR of 15–29 ml/min/1.73 m2) and metabolic acidosis (i.e., total CO2 < 22 mM) were randomly assigned to either daily sodium bicarbonate supplements (1 mEq/kg/day) or to an increase in dietary fruits and vegetables that was sufficient to reduce dietary acid by 50 %. After 1 year of treatment, the total CO2 had increased to a similar extent (compared to baseline values) in both the sodium bicarbonate and fruits plus vegetables groups. Regarding kidney functional outcomes, the eGFR calculated from plasma cystatin C levels did not differ between the groups but indices of kidney injury were lower in patients treated with diets enriched in fruits and vegetables.Fig. 1

Bottom Line:
Here we revisit how dietary factors could affect the treatment of patients with complications of chronic kidney disease (CKD), bringing to the attention of the reader the most recent developments in the field.We will briefly discuss five CKD-induced complications that are substantially improved by dietary manipulation: 1) metabolic acidosis and the progression of CKD; 2) improving the diet to take advantage of the benefits of angiotensin converting enzyme inhibitors (ACEi) on slowing the progression of CKD; 3) the diet and mineral bone disorders in CKD; 4) the safety of nutritional methods utilizing dietary protein restriction; and 5) evidence that new strategies can treat the loss of lean body mass that is commonly present in patients with CKD.

ABSTRACTHere we revisit how dietary factors could affect the treatment of patients with complications of chronic kidney disease (CKD), bringing to the attention of the reader the most recent developments in the field. We will briefly discuss five CKD-induced complications that are substantially improved by dietary manipulation: 1) metabolic acidosis and the progression of CKD; 2) improving the diet to take advantage of the benefits of angiotensin converting enzyme inhibitors (ACEi) on slowing the progression of CKD; 3) the diet and mineral bone disorders in CKD; 4) the safety of nutritional methods utilizing dietary protein restriction; and 5) evidence that new strategies can treat the loss of lean body mass that is commonly present in patients with CKD.